B15: Antibiotics and Painkillers
How antibiotics work, antibiotic resistance, drug development, and clinical trials
Key Definitions
Antibiotic — A medicine that kills bacteria inside the body (bactericidal) or stops them from reproducing (bacteriostatic). Antibiotics do NOT kill viruses.
Painkiller — A medicine that relieves symptoms (e.g. pain, fever, inflammation) but does NOT kill the pathogen or cure the disease.
Antibiotic resistance — When bacteria evolve to survive exposure to an antibiotic that previously killed them; resistant strains are harder to treat.
MRSA — Methicillin-resistant Staphylococcus aureus; a strain of bacteria resistant to several antibiotics, including methicillin.
Double-blind trial — A clinical trial where neither the patients nor the doctors know who receives the real drug and who receives the placebo.
Painkiller — A medicine that relieves symptoms (e.g. pain, fever, inflammation) but does NOT kill the pathogen or cure the disease.
Antibiotic resistance — When bacteria evolve to survive exposure to an antibiotic that previously killed them; resistant strains are harder to treat.
MRSA — Methicillin-resistant Staphylococcus aureus; a strain of bacteria resistant to several antibiotics, including methicillin.
Double-blind trial — A clinical trial where neither the patients nor the doctors know who receives the real drug and who receives the placebo.
Antibiotics: How They Work
Antibiotics kill or inhibit bacteria specifically:
— Bactericidal antibiotics kill bacteria (e.g. penicillin damages bacterial cell walls, causing them to burst).
— Bacteriostatic antibiotics stop bacteria from reproducing (e.g. tetracycline inhibits bacterial protein synthesis).
Why antibiotics cannot kill viruses:
— Viruses replicate inside human host cells, using the host's own cellular machinery.
— Antibiotics target prokaryotic features (cell walls, 70S ribosomes) that viruses do not have.
— To kill a virus, you would have to damage the human host cell — which would harm the patient.
— This is why antibiotics should NEVER be prescribed for viral infections (e.g. colds, flu).
— Bactericidal antibiotics kill bacteria (e.g. penicillin damages bacterial cell walls, causing them to burst).
— Bacteriostatic antibiotics stop bacteria from reproducing (e.g. tetracycline inhibits bacterial protein synthesis).
Why antibiotics cannot kill viruses:
— Viruses replicate inside human host cells, using the host's own cellular machinery.
— Antibiotics target prokaryotic features (cell walls, 70S ribosomes) that viruses do not have.
— To kill a virus, you would have to damage the human host cell — which would harm the patient.
— This is why antibiotics should NEVER be prescribed for viral infections (e.g. colds, flu).
Discovery of Penicillin
Alexander Fleming (1928):
— Fleming was growing bacteria on agar plates and noticed that mould (Penicillium notatum) had contaminated one plate.
— Around the mould, there was a clear zone where bacteria could not grow — the mould was producing a substance that killed bacteria.
— Fleming named this substance penicillin — the first antibiotic.
— Howard Florey and Ernst Chain later developed penicillin into a mass-produced medicine during World War II, saving millions of lives.
Penicillin works by preventing bacteria from forming normal cell walls. Without a strong cell wall, bacteria burst under their own internal pressure (osmotic lysis).
— Fleming was growing bacteria on agar plates and noticed that mould (Penicillium notatum) had contaminated one plate.
— Around the mould, there was a clear zone where bacteria could not grow — the mould was producing a substance that killed bacteria.
— Fleming named this substance penicillin — the first antibiotic.
— Howard Florey and Ernst Chain later developed penicillin into a mass-produced medicine during World War II, saving millions of lives.
Penicillin works by preventing bacteria from forming normal cell walls. Without a strong cell wall, bacteria burst under their own internal pressure (osmotic lysis).
Example 1: Why Antibiotics Cannot Treat Viral Infections
A patient with a cold (caused by a virus) asks for antibiotics. The doctor should refuse because antibiotics only target bacterial structures (cell walls, ribosomes, DNA replication). Viruses have no cell wall, no independent metabolism, and replicate inside human cells using the host's machinery. Antibiotics have no target in a virus and would be ineffective. Additionally, inappropriate antibiotic use contributes to antibiotic resistance.
Example 2: How Penicillin Kills Bacteria
Penicillin interferes with the enzymes that build the peptidoglycan cell wall of bacteria. Without a properly formed cell wall, the bacterium cannot withstand the osmotic pressure from water entering by osmosis. The bacterial cell swells and bursts (lysis). Penicillin only affects dividing bacteria that are actively building new cell walls. Human cells are unaffected because they have no cell walls.
Antibiotic Resistance
How antibiotic resistance arises (by natural selection):
1. Mutation — Random mutations in bacterial DNA can produce resistance genes (e.g. a gene for an enzyme that breaks down the antibiotic).
2. Variation — Within a bacterial population, some individuals carry the resistance mutation and some do not.
3. Selection pressure — When the antibiotic is used, susceptible bacteria are killed, but resistant bacteria survive.
4. Survival and reproduction — Resistant bacteria survive, reproduce by binary fission, and pass the resistance gene to their offspring.
5. Plasmid transfer — Resistance genes on plasmids can be transferred between bacteria (horizontal gene transfer), spreading resistance rapidly.
6. Over time, the resistant strain becomes more common — this is evolution by natural selection.
MRSA (Methicillin-resistant Staphylococcus aureus):
— A strain of S. aureus that has evolved resistance to methicillin and several other antibiotics.
— Common in hospitals where antibiotics are used frequently and people have weakened immune systems.
— MRSA infections are harder and more expensive to treat, requiring stronger "last resort" antibiotics.
1. Mutation — Random mutations in bacterial DNA can produce resistance genes (e.g. a gene for an enzyme that breaks down the antibiotic).
2. Variation — Within a bacterial population, some individuals carry the resistance mutation and some do not.
3. Selection pressure — When the antibiotic is used, susceptible bacteria are killed, but resistant bacteria survive.
4. Survival and reproduction — Resistant bacteria survive, reproduce by binary fission, and pass the resistance gene to their offspring.
5. Plasmid transfer — Resistance genes on plasmids can be transferred between bacteria (horizontal gene transfer), spreading resistance rapidly.
6. Over time, the resistant strain becomes more common — this is evolution by natural selection.
MRSA (Methicillin-resistant Staphylococcus aureus):
— A strain of S. aureus that has evolved resistance to methicillin and several other antibiotics.
— Common in hospitals where antibiotics are used frequently and people have weakened immune systems.
— MRSA infections are harder and more expensive to treat, requiring stronger "last resort" antibiotics.
Example 3: Natural Selection and Antibiotic Resistance
When a patient takes an antibiotic for a bacterial infection, most bacteria are killed. However, if a few bacteria carry a mutation that makes them resistant to the antibiotic, these survive. With the competing non-resistant bacteria removed, the resistant bacteria can reproduce freely by binary fission. Within a short time, the entire population may be resistant. The antibiotic acted as a selection pressure, favouring the resistant strain.
Reducing Antibiotic Resistance
How to slow the development of antibiotic resistance:
— Only prescribe antibiotics when necessary — not for viral infections or mild bacterial infections that the immune system can clear.
— Complete the full course — Even if symptoms improve, all bacteria must be killed to prevent the survival of partially resistant bacteria.
— Restrict agricultural use — Antibiotics should not be used as growth promoters in livestock farming.
— Develop new antibiotics — However, this is expensive and slow; few new antibiotics have been discovered recently.
— Infection control — Good hygiene in hospitals reduces the spread of resistant strains.
— Targeted treatment — Use specific antibiotics rather than broad-spectrum ones when the pathogen is identified.
— Only prescribe antibiotics when necessary — not for viral infections or mild bacterial infections that the immune system can clear.
— Complete the full course — Even if symptoms improve, all bacteria must be killed to prevent the survival of partially resistant bacteria.
— Restrict agricultural use — Antibiotics should not be used as growth promoters in livestock farming.
— Develop new antibiotics — However, this is expensive and slow; few new antibiotics have been discovered recently.
— Infection control — Good hygiene in hospitals reduces the spread of resistant strains.
— Targeted treatment — Use specific antibiotics rather than broad-spectrum ones when the pathogen is identified.
Example 4: Why Completing the Full Course Matters
If a patient stops taking antibiotics early because they feel better, the weakest bacteria have been killed but the more resistant ones may still be alive. These surviving bacteria are more resistant to the antibiotic than the original population. If they reproduce, the new infection will be harder to treat. Completing the full course ensures even the more resistant bacteria are killed, preventing the selection of partially resistant strains.
Painkillers and Other Drugs
Painkillers (e.g. paracetamol, ibuprofen, aspirin) relieve symptoms but do NOT kill pathogens or cure the disease:
— They reduce pain, lower fever, and reduce inflammation.
— They do not affect the pathogen, so the immune system must still clear the infection.
— For bacterial infections, painkillers may be used alongside antibiotics to manage symptoms while the antibiotics kill the bacteria.
Other drugs:
— Antivirals — Can inhibit viral replication (but are difficult to develop; they do not "kill" viruses like antibiotics kill bacteria).
— Antifungals — Treat fungal infections (e.g. athlete's foot, thrush).
— Antimalarials — Treat or prevent malaria (protist infection).
— They reduce pain, lower fever, and reduce inflammation.
— They do not affect the pathogen, so the immune system must still clear the infection.
— For bacterial infections, painkillers may be used alongside antibiotics to manage symptoms while the antibiotics kill the bacteria.
Other drugs:
— Antivirals — Can inhibit viral replication (but are difficult to develop; they do not "kill" viruses like antibiotics kill bacteria).
— Antifungals — Treat fungal infections (e.g. athlete's foot, thrush).
— Antimalarials — Treat or prevent malaria (protist infection).
Drug Development and Testing
Stages of drug development:
1. Discovery/preclinical testing — The drug is tested on human cells and tissues in the lab, then on animals (to check for toxicity, efficacy, and dosage).
2. Clinical trials — Phase 1 — Tested on a small number of healthy volunteers to check for safety and side effects.
3. Clinical trials — Phase 2 — Tested on a small number of patients with the disease to check for efficacy (does it work?).
4. Clinical trials — Phase 3 — Large-scale testing on hundreds or thousands of patients; compared to existing treatments.
Double-blind trials:
— Patients are randomly assigned to the experimental group (receives the new drug) or the control group (receives a placebo or the current best treatment).
— Neither the patients NOR the doctors know who is in which group until the trial ends.
— This eliminates bias — the placebo effect and the doctor's expectations cannot influence results.
1. Discovery/preclinical testing — The drug is tested on human cells and tissues in the lab, then on animals (to check for toxicity, efficacy, and dosage).
2. Clinical trials — Phase 1 — Tested on a small number of healthy volunteers to check for safety and side effects.
3. Clinical trials — Phase 2 — Tested on a small number of patients with the disease to check for efficacy (does it work?).
4. Clinical trials — Phase 3 — Large-scale testing on hundreds or thousands of patients; compared to existing treatments.
Double-blind trials:
— Patients are randomly assigned to the experimental group (receives the new drug) or the control group (receives a placebo or the current best treatment).
— Neither the patients NOR the doctors know who is in which group until the trial ends.
— This eliminates bias — the placebo effect and the doctor's expectations cannot influence results.
Example 5: The Thalidomide Tragedy
Thalidomide was developed in the 1950s as a sleeping pill and was later prescribed to pregnant women for morning sickness. It had not been adequately tested on pregnant animals. The drug crossed the placenta and caused severe limb deformities (phocomelia) in over 10,000 babies worldwide. This tragedy led to much stricter drug testing regulations, requiring thorough testing for teratogenicity (ability to cause birth defects) before any drug can be licensed.
Exam tip: Always distinguish between antibiotics (kill bacteria, cure the disease) and painkillers (relieve symptoms only, do not kill the pathogen). When explaining antibiotic resistance, use the language of natural selection: mutation → variation → selection pressure → survival of resistant individuals → reproduction → increase in resistant population.
Practice Questions
1. Foundation Explain why antibiotics cannot be used to treat viral infections.
Antibiotics target prokaryotic features such as bacterial cell walls, ribosomes, and DNA replication machinery. Viruses are not cells — they have no cell wall and no independent metabolism. They replicate inside human host cells using the host's cellular machinery. To kill a virus, you would have to damage the human host cell, which would harm the patient. Therefore, antibiotics have no target in a virus and are ineffective against viral infections.
2. Higher Explain how antibiotic resistance arises through natural selection.
Random mutations in bacterial DNA can produce resistance genes. When an antibiotic is used, it kills susceptible bacteria but resistant bacteria survive (the antibiotic is a selection pressure). The surviving resistant bacteria reproduce by binary fission, passing the resistance gene to their offspring. Resistance genes on plasmids can also be transferred between different bacteria. Over time, the resistant strain becomes more common in the population — this is evolution by natural selection.
3. Foundation Describe the difference between antibiotics and painkillers.
Antibiotics kill bacteria or stop them from reproducing — they cure the disease by removing the cause. Painkillers only relieve symptoms (pain, fever, inflammation) but do not kill the pathogen or cure the disease. The immune system must still clear the infection even when painkillers are used.
4. Higher Explain what a double-blind trial is and why it is important in drug testing.
In a double-blind trial, neither the patients nor the doctors know who receives the real drug and who receives the placebo. This is important because it eliminates bias. If patients knew they were receiving the real drug, they might report improvement due to the placebo effect. If doctors knew, they might unconsciously interpret results more favourably for the real drug. By keeping both groups "blind," the results are objective and reliable.
5. Higher Describe three ways to reduce the development of antibiotic resistance.
1) Only prescribe antibiotics when they are genuinely needed (not for viral infections or mild bacterial infections). 2) Patients must complete the full course of antibiotics to ensure all bacteria are killed, preventing partially resistant bacteria from surviving. 3) Restrict the use of antibiotics in agriculture (not used as growth promoters in livestock). Also acceptable: develop new antibiotics, practise good hygiene in hospitals, use targeted (narrow-spectrum) antibiotics.
6. Foundation Describe how penicillin was discovered and how it kills bacteria.
Alexander Fleming discovered penicillin in 1928 when he noticed that mould (Penicillium) growing on a bacterial culture plate had created a clear zone where bacteria could not grow. The mould produced a substance (penicillin) that killed the bacteria. Penicillin works by damaging bacterial cell walls — it prevents the formation of peptidoglycan, so the cell wall is weak and bacteria burst under osmotic pressure. Human cells are unaffected because they have no cell walls.
🔢 Maths Skills
Mathematical Skills
Interpreting antibiotic resistance trend data: plot and analyse graphs showing the percentage of bacterial infections that are resistant to an antibiotic over time. Calculate percentage increase in resistance rates and compare trends between different antibiotics.
⚠️ Common Misconceptions
Watch Out!
1. Wrong: Antibiotics kill viruses Correct: Antibiotics only kill bacteria — they target bacterial structures like cell walls and ribosomes that viruses do not have
2. Wrong: You should stop taking antibiotics early if you feel better Correct: You must complete the full course to ensure all bacteria are killed, otherwise the surviving partially resistant bacteria can reproduce and create a resistant strain
✍️ 6-Mark Question
Extended Answer
6 marks: Explain how antibiotic resistance develops and its implications.
Antibiotic resistance develops through natural selection. Random mutations in bacterial DNA produce resistance genes. When an antibiotic is used, susceptible bacteria are killed but resistant bacteria survive (the antibiotic acts as a selection pressure). The resistant bacteria reproduce by binary fission, passing the resistance gene to offspring. Resistance genes on plasmids can also transfer between bacteria horizontally. Over time, the resistant strain becomes more common. The implications are serious: infections become harder and more expensive to treat, existing antibiotics become ineffective, and diseases like MRSA can spread in hospitals. Few new antibiotics are being developed, making this a major global health threat.
Mark scheme: 1 mark for mutation producing resistance gene; 1 mark for antibiotic as selection pressure; 1 mark for survival of resistant bacteria; 1 mark for reproduction and gene transfer (plasmids); 1 mark for implications (harder to treat, MRSA); 1 mark for QWC (uses natural selection terminology correctly)
📊 AO3: Analyse & Evaluate
Analysis and Evaluation
A hospital recorded the following data on MRSA infections: 2018: 45 cases, antibiotic use in 80% of patients; 2019: 38 cases, antibiotic use in 65% of patients; 2020: 22 cases, antibiotic use in 50% of patients; 2021: 18 cases, antibiotic use in 45% of patients. Hand hygiene compliance also increased from 70% (2018) to 95% (2021).
1. Calculate the percentage decrease in MRSA cases from 2018 to 2021. 2. Suggest why reducing unnecessary antibiotic use helps reduce MRSA. 3. Evaluate the relative importance of reduced antibiotic use versus improved hand hygiene in controlling MRSA, using the data provided.
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